Chapter 1 (Cell Injury) - 1-1 (~7:00) - cell injury 1

Chapter 2 (Inflammation and Repair) - 1-4 (~6:37) Inflammation 2

Chapter 3 (immunopathology) - (not covered except during endocrine)
Chapter 4 (water, elec., acid-base) - 1-5 (~31:10) Fluid/Hemody 1
Chapter 5 (genetic and developmental disorders) mixed/not covered
Chapter 6 (environmental pathology) mixed/not covered
Chapter 7 (Nutritional disorders) - 2-1 (~2:50) Nutrition 1
Chapter 8 (Neoplasia) - 2-2 (~31:21) Nutrition 2
Chapter 9-10 (vascular and heart disorders) - 3-3 (~37:15) Hemato 8
Chapter
Chapter
Chapter
Chapter
Chapter

11
12
13
14
15

(RBC disorders) - 2-4 (~31:38) Neoplasia 3

(WBC disorders) - 2-7 (~44:10) Hemato 4
(lymphoid disorders) - 2-8 (~42:34) Hemato 5
(hemostasis disorders) - 3-1 (~17:04) Hemato 6
(Blood banking and transfusion) - 3-2 (~42:13) Hemato 7

Chapter
Chapter
Chapter
Chapter
Chapter
Chapter
Chapter
Chapter
Chapter
Chapter
Chapter

16
17
18
19
20
20
21
22
23
24
25

(Upper N Lower respiratory) - 3-8 (0:00) Respiratory 1

(Gastrointest. disorders) - 4-2 (~13:00) Respiratory 3
(Hepatobiliary and Pancreatic) - 4-4 (~29:30) GI 2
(kidney disorders) - 4-6 (~24:40) Hepato/pancreas 2
(lower urinary tract) - 4-8 (~39:21) Renal 2
(male reproductive tract) - 4-8 (~44:50) Renal 2
(female reproductive and breast) - 5-1 (0:00) Gyn 1
(endocrine) - 5-2 (0:00) Gyn 2
(musculoskeletal) - 5-4 (~10:39) Musculoskeletal
(skin disorders) - 5-5 (~14:56) - Skin
(nervous system) - 5-5 (~34:04) Skin

Hydrocephalus
MCC = stenosis of the aqueduct of sylvius, which would be
noncommunicating. Theyget hydrocephalus because the sutures have not
fusedif you miss hydrocephalus in adult and sutures have fused, will lead to
dilatation of the ventricles and eventually over years, the pressure will turn
back to normal because the increased pressures will keep the choroid plexus
from making so muchbut the damage has been done the ventricles are

dilated and you can get dementia, ataxia, related urinary incontinence.Aka
normal pressure hydrocephalus (because pressures normalize)
Tuberous Sclerosis
AD
Hamartomas (noneoplastic proliferation of things). Ventricles have bumps
called tubercles which are hamartomas which have proliferation of
astrocytes. They produce hamartomas that bulge into the ventricle, called
candle stick dripping. Hemartomas of the kidney called angiomyolipomas,
MR, cardiac tumors (rhabdomyomas), shagreen patches, areas of
hypopigmentation, woods light shine out
AnencephalyWorst of neural tube defects. Absent brain
Vertebral arch defects
Spina bifida occulta tufts of hair come out, vertebral arches do not touch,
no meninges come
Meningoceole meninges come out
Meningomylocele both meninges and spinal cord come out. High alpha
feto protein levels in blood of mother; decreased alpha feto protein in downs
syndrome
Have to be on folate to prevent neural tube defects (neural tube finished
forming by 26-30 days, so make sure she is on folate if she is trying to get
pregnant).
Neurofibromatosis
Albright syndrome (precocious puberty, caf au lait, bone zits)Sturge
weberCaf au lait (coffee colored non raised lesions) spot, plexiform
neurofibromas, hyperpigmentation in the axilla (axillary freckling),
neurofibromasAD , therefore late manifestations (esp for neurofibromatosis),
penetrance, variable expressivity (you are expressing the disease, but diff
levels of how severe the disease is)
Tumors of PNS and CNS
One is more common
Example: pt with HTN and pic, what test would you get? Relationship of
neurofibromatosis with pheochromocytoma, therefore get a 24 hr urine for
VMA and metanephrine.
Acoustic schwannoma (NF type 2)

Example: pt with sensorinerual hearining loss benign tumor of Schwann

cells around CN 8
Meningiomas (NF type 1)
Optic nerve gliomas, benign tumor of optiv nerve
Syringomyelia
Example: pt that works in factory and one of workers says you are burning
your hand and pt didnt notice this, on exam loss of musculature (loss of
LMN) in intrinsic muscles of the hand, loss of pain and temp in cape like
distribution across shoulder.
Big cystic cavity knocking off spinothalamic knocking off pain and temp. can
knock off the corticospinal tract and anterior horn cells, so it will be a COMBO
of sensory AND motor loss for syringiomyelia. They have bladder problems.
Infections
Cant feel pain (not ALS in ALS, first place of development of loss of
intrinsic muscles is here, so dont confuse; but ALS is UMN and LMN, pure
motor problem! ) and not sensory!
Meningitis vs encephalitis
Meningitis is the inflammation of the meninges and youll have nuchal rigidity
If you move your head or extend your knee, you will stretch the meninges, it
hurts!
Encephalitis sleeping sickness they are always sleeping and drowsy; they
have mental status abnormalities (not nuchal rigidity).
Pus at the base of the brain can possibly block lushka and majendie,
leading to obstructive hydrocephaly and noncommunicating! When you treat
meningitis, use steroids and antibiotics. why? Steroids prevent scar tissue
formation and complications that arise with it (ie hydrocephalus).This is
standard TB meningitis treatment (TB in brain causes vasculitis, infarctions
and scarring)

Deafness is a complication of meningitis.

Rabies
Example:: meningitis, cerebral abcess, Rabies (MCC in United States =
skunks is the number one cause, dogs in third world), Negri bodies (purkinje
cell inclusion)

This kid has a congenital infection, when they took X-ray they saw a peculiar
abnormality and the kid dies! It is periventricular calcification! Begins with
encephalitis
CMV
Periventricular calicificationsExample: section of kid (brain) - see white stuff
going around ventricles MC congental infection = CMV
What body fluid is best to culture from? Urine
Meningitis
What is MC meningitis/sepsis in first month of life? Group B strep strep
agalactiae because many women have this organism in their vagina, so
they are carriers. Premature ruptured of the membranes lets the organism
get up, get an chorioamnionitis and into the bloodstream of the newborn
Number 2 cause is E.coli
Third is Listeria monocytogenes- (gram + rod with tumbling motility as
does Trichomonas vaginalis)
What food should pregnant women avoid? Soft cheeses (ie feta cheese, but
listeria monocytogenes is present in some cheeses).
MC in 1 month 18 yo = N. meningitides
(not H influenza because of vaccination)
MC in 18+ = Strep pn
Example: 52 yo man, nuchal rigidity, tap shows increased protein, increased
neutrophils and decreased glucose dx? Strep pn. what is the gram stain?
Gram + diplococcus
Cryptococcus
Pigeons. India ink see narrow based bud for Cryptococcus. Bud based
Blasto
Who do you think this is in? immune-compromised pts
What is MC immunodef in USA? AIDsMCC meningitis in AIDs pts?
Cryptococcus
Mucormycosis
In frontal lobe, therefore from a diabetic in ketoacidosisExample: special
stain on AIDs pt with CD 4 ct of 50, CT showed space occupying lesion ..Dx?

ToxoplasmosisExample: pig herder, and long time problem with focal

epileptic seizures (dilating therapy) multiple calcified and cystic lesions
inbrain dx? CysticercosisExample: Jacob Cruetzfeltds from prions (mad
cow) who is most likely to get? Neuropathologists, neurosurgeons, beef,
lettucefrom Arizona (cow manure on it).
Traumatic lesionsEpidural hematoma (sitting above dura) hit in head
tempo-parietal lobe and middle meningeal have to fracture bone (under
arterial pressures, can separate dura from periosteum) and it takes about 6
hrs and when you get 50 mls of blood, you get uncal herniation and die. Ie
get him, say they are ok, 6 hrs later epidural hematoma and death
Subdural hematoma rupture of bridging veins between dura and
arachnoid membrane. If you have cerebral atrophy like older and alcoholics
then the space between the dura and arachnoid membranes is bigger.
Bridging veins dangling, break and get a hematoma. Fluctuating levels of
consciousness. Left untreated lead to dementia. Do CT (pick up blood) to rule
out epi and subdural hematoma (also for strokes if its a hemorrhagic
stroke)heparin if blood is not there!
Strokes
Brain: one side is bigger.
There is break down of white matter this is an atherosclerotic stroke; pale
infarct of brain, there is no hemorrhage in it. At bifurcation, there is an
atherosclerotic plaque and thrombus. No blood flow to the brain and it
infracted, starts breaking down, no reperfusion, the thrombus doesnt resolve
so it remains a pale infarct. If the thrombus did break apart, and reperfuse
the brain, the blood in the goes into the area of infarction and is called a
hemorrhagic infarct. However, this usually doesnt occur and pale infarcts
more common. If no blood, and there is infarction, pt is a candidate for
heparin therapy. Over time, if pt survives, ends up with cystic space where
there was infarction and this is called liquefactive necrosis--pale infarct,
liquefactive necrosis.
Meningitis inflammation of meninges and nuchal rigidity leading to pain
(stretching inflamed meninges).

MCC is E coli

MCC is listeria monocytogenes

Hemorrhagic infarct blood is to edge of brain this is an embolic infarct,
usually from left side of the heart. The vessel it always goes to is middle
cerebral artery. It gets into the Circle of Willis and into the middle cerebral. If
you embolize down, will go into the superior mesentericartery. The reason it
is hemorrhagic is because patient will get breakdown of fibrinolytic system of
the embolus and leads to reperfusion. Instead of being a pale infarct, its a
hemorrhagic infarct. So, both a atherosclerotic stroke and hemorrhagic

stroke are both infarcts one is pale and the other is hemorrhagic.
HTN, pressures cause lenticulostriate vessels to come up and supply this
area of the brain. Derive from the middle cerebral aneurysms, called
Charcot Bouchard aneurysm and it ruptures, leading to giant hematoma
and blood clot. It ruptures and it has horrible prognosis.So, embolic stroke
goes to surface of the brain, clot in basal ganglia or putamen and if its in the
basal ganglia, its always an intracebral bleed from HTN.
Example: subarachnoid hemorrhage mostly due to rupture congenital
berry aneurysm. MC at the junction ant communicating branch of anterior
cerebral artery. Less common cause of SAH:AV malformation
Sturge Weber on same side as skin lesion of the face, there is an AV
malformation
Lacunar infarcts small areas on the brain; unusual because they hit
areasof the brain. Depending on where in the internal capsule, can have a
pure motor stroke or pure sensory as opposed to combination. Pure motor or
sensory! MC due to HTN
Multiple Sclerosis (MS)MC demyelinating Disease (autoimmune) MS
Demylinated: white matter has myelin it, grey matter doesnt. If you are
destroying white matter, then youll see grey matter underneath. Plaques of
MS.
2 ways to demyelinate1) knock off cell that makes myelin in the brain
(oligodendrocytes in brain, schwann cell in PNS) viruses do this subacute
sclerosis, progressive multifocal leukoencephalopathy, HPV they affect the
oligodendrocyte and produce demyelination.
2) can also have Abs against myelin and not the oligodendrocyte, which is
MS, Paresthesias, Nystagmus, ataxia, optic neuritis with blurry vision (MCC
of Optic Neuritis= MS because demyelination of optic nerve)
they look at the right, jerk nystagmus and left eye looking at you
Internuclear opthalmaplegia (demyelination of MLF) pathognomonic MS
Spinal tap will show increased protein, normal glucose, increase
lymphocytes of autoimmune disease
Hydrocephalus Ex Vacuo
There is no cerebral cortex. There is severe atrophy of brain and ventricles
look bigger than they should be Dementia
Alzheimers Disease

Classic lesion: senile plaque, neurits, beta bamyloid (Beta!!) so beta

amyloid is toxic and the more you have the more toxic to neurons
pathognomonic of alzheimers, on chromosome 21, therefore seen in downs,
neurofibriillary tangles (in any dementia and HD)Alz probs in higer levels
dementiaOnly way to dx is autopsy (confirmation) see senile plaques
Parkinsons Diease
Resting tremor

Psychology and autopsy!

UWORLD questions

The pathogenesis of prion disease is described in this question.

The most well known examples of prion disease are CreutzfeldtJakob disease in humans and Bovine Spongiform encephalopathy
(mad cow disease) in cattle.
Prion protein is normally found in neurons and has alpha-helical
structure, if the conversion of alpha

When disease incidence increases, sensitivity and specificity screening

remain same. Screening tests are indicative of prevalence
More people have the disease, sensitivity does not change and
specificity has no change at all
Prevalence means simply more disease changes, ratio stays constant
Prevalence increase or decrease- no change effect on pretest
probability
The positives increase so do negatives correspondingly
They are locked- sensitivity and specificity
Prevalence increases PPV increases and negative predictive
value decreases
Ratio will change mathematically
You cant get predictive value without prevalence
Optimum sensitivity this is about detecting disease

E is the point of optimum sensitivity

Optimum specificity- C, ALL the way to the right is healthy people
Highest PPV what is positive predictive value- you have the disease,
yes you have the disease- c over every person is disease 100% have
the disease and so that is point C to the left!
Now for the highest NPV- e over to the right you have nothing but
healthy people, perfect negative predictive value.when I label someone
as healthy im positive sure that im correct
Sensitivity and ppv are inversed and specificity and nnv are inversed
Sensitivity and negative predictive value paired and specificity and
positive predictive value are paired
Sensitivity is true positive rate
1-specificity is false positive rate
whichever curve bows more to the upper left corner is the best
screening test
highest accuracy, also 6 as before.
Mathematically, area under each curve gives you accuracy
Higher sensitive value means yes you find a lot of people with disease,
however that combined with lower predictive value indicates that there
are a lot of false positives and so youll be detecting many people who
may actually not have the disease
Youll miss people who have the disease. Positive ppv and people have
the disease but miss lower sen
There are two types of studies- observational and experimental studies
Observational- simply observing
Experimental studies- clinical trials, there is an intervention
Experimental studies- intervention!
Headache with pupil dilated is an aneurysm, mostly posterior
communicating artery if proven otherwise
Meningitis can trap, mostly TB meningitis cause cn 3 damage
Subarchanoid infiltration by malignancy
Ischemic lesions occur when there is microangiopathy macrovessel
disease
Ischemia leads to somato fiber
Cavernous sinus thrombosis if you see a dysfunction of the cranial
nerve three, with abducens, or trochlear, or V1 and V2

Internal carotid artery aneurysm or explosion of i.c.a. called carotico

cavernous fistula
Pitutuary adenoma affect third nerve and pituary apoplexy (loose their
own nerve supply)